This article reviews the data on a unique, rare rheumatologic syndrome osteoarthropathy of the anterior thorax (OAAT), characterized by inflammation of the bone, joint, and ligament structures that form the skeleton of the anterior thorax. OAAT is part of chronic non-bacterial osteomyelitis, which occurs in adults and children and may be due to genetic mutations. The basis of this disorder is osteitis (focal lesion of the sternum, clavicles, and ribs with a tendency to the destruction of mainly articular parts and development of bone proliferation hyperostosis), arthritis with possible ankylosis development, as well as enthesitis and ligamentitis with ectopic ossification of affected soft tissues. Many patients also show similar dermatological changes: commonly palmar and plantar pustulosis and sometimes acne inversa (purulent hidradenitis and globular acne). The article describes typical radiological, scintigraphic, and MRI changes in the musculoskeletal system. The classification of chronic non-bacterial osteomyelitis is reviewed. Diseases that may mimic OAAT are listed. Treatments for chronic non-bacterial osteomyelitis, including bisphosphonates and biologics, are reported.

A review of data on the possible causes of an increase rheumatoid factor (RF), antibodies against cyclic citrullinated peptide (ACCP) and antibodies to modified citrullinated vimentin (AMCV) in patients without rheumatoid arthritis (RA) is presented. The possibility of hyperproduction of these autoantibodies before the development of the clinical picture of RA was indicated. It is indicated that ACCP and IgA RF have the greatest prognostic value in terms of the subsequent development of RA. These antibodies are recommended to be additionally determined in diagnostically difficult cases. Data on the sensitivity and specificity of detection of RF, ACCP and AMCV in the diagnosis of RA are summarized. The results of detection of the discussed antibodies in various rheumatic (other than RA) and non-rheumatic diseases are presented in detail. Particular attention is paid to diseases in which increased synthesis of RF, ACCP and AMCV may not be accompanied by clear clinical symptoms (Sjögren’s disease, autoimmune thyroiditis, some chronic infections, silicosis, monoclonal gammopathy, etc.). Recommendations are given for examining patients with “accidentally” identified increase in RF or ACCP.

An analysis of causes leading to pain recurrence in patients with polymyalgia rheumatica (PR) after tapering down the dose of glucocorticosteroids (GCS) is presented. True exacerbations resulting from the main disease recurrence and pseudo-exacerbations when the resumption of pain syndrome is not due inflammation but because of other causes – steroid myopathy or chronic adrenal insufficiency (AI) are identified. The experience of using tocilizumab, an inhibitor of interleukin-6 receptors, as steroid-sparing agent in patients with PR is considered. The factors contributing to pain syndrome development, which can mimic exacerbations of PR (associated myofascial pain, vitamin D deficiency, etc.) are indicated. The methodology for AI diagnosis in patients receiving GCS therapy is discussed in detail. Recommendations for the rational AI therapy including acute cases are given.